Elsevier

Peptides

Volume 17, Issue 3, 1996, Pages 517-520
Peptides

Article
Neuropeptide Y blocks and reverses interleukin-1β-induced anorexia in rats

https://doi.org/10.1016/0196-9781(96)00016-2Get rights and content

Abstract

Neuropeptide Y (NPY) increases feeding by direct action in the central nervous system (CNS). Interleukin-1β (IL-1β), on the other hand, induces anorexia when administered ICV at estimated pathophysiological (e.g., yielded by 1.0 ng/rat dose) and pharmacological (≥4.0 ng) concentrations in the cerebrospinal fluid (CSF). In the present study, we investigated NPYIL-1β interactions using the ICV administration. ICV microinfusion of NPY (5.0 μg) significantly increased 2-h food intake (by 89%), whereas IL-1β decreased 2-h food intake (32% decrease with 1.0 ng/rat; 53% with 4.0 ng/rat; and 51% with 8.0 ng/rat). NPY (5.0 μg) blocked the anorexic effect induced by all doses of IL-1β when both compounds were administered concomitantly. Central infusion of NPY was also able to induce feeding in IL-1β-pretreated rats exhibiting marked anorexia. The results show that ICV-administered NPY blocks and reverses the anorexia induced by estimated pathophysiological and pharmacological concentrations of IL-1β in rats. A second interpretation of a data subset is that IL-1β attenuates or blocks NPY-induced increase in feeding depending on the IL-1β dose used. Blockage and reversal of IL-1β-induced anorexia by NPY suggest the importance in studying cytokine-peptide interactions in the regulation of feeding behavior. Understanding these endogenous interactions may produce strategies with potential therapeutic implications for chronic diseases associated with long-term anorexia.

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    Pro-opiomelanocortin (POMC) neurons and neuropeptide Y (NPY) in the arcuate nucleus of the hypothalamus are the main regulators of appetite and energy expenditure [5]. Intracerebral administration of IL-1β antagonizes NPY-induced feeding in rats by specifically reducing NPY mRNA levels, and NPY also prevents and reverses IL-1β-induced anorexia [6,7]. This suggests an interplay of cytokine-neuropeptides in anorexia nervosa.

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    For example, ip IL-1ß administration increases NPY levels in the PVH, but not in the ARH, which can reflect inhibition of NPY release (McCarthy et al., 1995). Moreover, intracerebroventricularly infused NPY can counter the reduction of food intake after IL-1β administration (Sonti et al., 1996). Collectively, these findings indicate that IL-1β acts on NPY-containing neurons to inhibit its release and thus favor hypophagia.

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